AKT1 and gastroesophageal reflux disease: In a reflux esophagitis rat model, activation of the PI3K/Akt pathway was associated with oxidative stress and inflammatory injury; inhibition of this pathway alleviated inflammation and oxidative damage, thereby improving symptoms of reflux esophagitis.[22] In the early stages of IS, PI3K/Akt activation promotes neuronal survival and regeneration, mitigates brain tissue injury, and exerts neuroprotective effects.